PTBP1 Targets ILK to Regulate the Hypoxia-Induced Phenotypic Transformation of Pulmonary Artery Smooth Muscle Cells.

Purpose: Pulmonary hypertension (PH) is a pathological process mainly characterized by the progressive increase in pulmonary vascular resistance. The degradation of pulmonary artery smooth muscle cells (PASMCs) from contractile/differentiated phenotype to synthetic/dedifferentiated phenotype is a key factor for hypoxic pulmonary hypertension.

Materials And Methods: In this study, qPCR was performed to evaluate the gene expression of mRNAs.

miR-142 is a Sensitive Biomarker for the Diagnosis and Prognosis of Acute Myocardial Infarction.

Background: Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of coronary arteries. AMI is one of the most common diseases in European countries and over 1.5 million AMI patients die of it in the United States annually.

MSCs Contribute to the Conversion of Ly6C Monocytes into Ly6C Subsets under AMI.

Background: Ly6C monocytes are inflammatory cells that accumulate in an infarcted myocardium, and Ly6C monocytes are believed to be reparative and curb myocardial remodeling. NR4A1 is a novel target for modulating the inflammatory phenotype of monocytes during atherogenesis.

Objectives: We aimed to investigate whether MSCs can contribute to the heterogeneity of Ly6C monocytes differentiated into Ly6C monocytes and whether this regulation is related to nuclear receptor NR4A1.

Protease-activated receptor 2 deficiency in hematopoietic lineage protects against myocardial infarction through attenuated inflammatory response and fibrosis.

Ischaemic heart disease is one of the leading causes of death. Protease-activated receptor 2 (PAR2) is widely expressed within the cardiovascular system and is known to mediate inflammatory processes in various immunocytes, such as macrophages, mastocytes and neutrophils. Here, we investigated whether activating macrophage PAR2 modulates cardiac remodelling in a murine model of myocardial infarction.

LncRNA-LUNAR1 Levels Are Closely Related to Coronary Collaterals in Patients with Chronic Total Coronary Occlusion.

Coronary collaterals can effectively improve myocardial blood supply to the area of CTO (chronic total coronary occlusion) and can, thus, reduce infarct size. LUNAR1(leukemia-induced noncoding activator RNA-1) is a specific LncRNA regulated by Notch signaling that not only can enhance the expression of IGFR-1 but also can promote angiogenesis and cell survival. Here, we investigated the relationship between LncRNA-LUNAR1 levels in peripheral plasma and the formation of coronary collaterals.

Tetramethylprazine attenuates myocardial ischemia/reperfusion injury through modulation of autophagy.

The current study aimed to investigate the effects of tetramethylprazine (TMP) on myocardial ischemia/reperfusion (MI/R) injury and its underlying mechanisms. MI/R rat model and hypoxia/reoxygenation (H/R) cardiomyocytes model were established. CK level and LDH activity were detected to evaluate MI/R and H/R injury.

miR-17 regulates the proliferation and apoptosis of endothelial cells in coronary heart disease via targeting insulin-like-growth factor 1.

Coronary heart disease (CHD) is one of the main risks of death, which is mainly caused by coronary arteries arteriosclerosis. The present study aims to investigate the potential roles of miR-17 in CHD. In the present study, Human umbilical vascular endothelial cells (HUVECs) were treated with oxidized low density lipoprotein (ox-LDL).

Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p.

Atherosclerosis (AS) is a chronic inflammatory disease threatening human health, and vascular smooth muscle cells (VSMCs) are involved in AS processes. Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on AS.

MicroRNA-7b attenuates ischemia/reperfusion-induced H9C2 cardiomyocyte apoptosis via the hypoxia inducible factor-1/p-p38 pathway.

Objective: MicroRNAs (miRNAs) have been shown to play crucial roles in the occurrence, development, and treatment of many cardiovascular diseases. Coronary heart disease (CAD)-related miRNAs are still a growing research area. miR-7b was reported to be downregulated in acute myocardial infarction (AMI) myocardium tissues.

Advanced glycation end products of bovine serum albumin affect the cell growth of human umbilical vein endothelial cells via modulation of MEG3/miR-93/p21 pathway.

Advanced glycation end products of BSA (AGE-BSA) contribute to the pathogenesis of diabetic vascular diseases. However, the roles and underlying mechanisms of AGE-BSA in diabetic vascular diseases remain largely unclear. Long non-coding RNAs (lncRNAs) are widely identified and known as gene regulators.

DNA methylation regulates α-smooth muscle actin expression during cardiac fibroblast differentiation.

Cardiac fibroblast (CF) differentiation to myofibroblasts expressing α-smooth muscle actin (α-SMA) plays a key role in cardiac fibrosis. Therefore, a study of the mechanism regulating α-SMA expression is a means to understanding the mechanism of fibroblast differentiation and cardiac fibrosis. Previous studies have shown that DNA methylation is associated with gene expression and is related to the development of tissue fibrosis.

TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14-NF-κB signaling pathway.

Acute myocardial infarction (AMI) remains one of the leading causes of mortality worldwide; however, endothelial progenitor cell (EPC) transplantation has been proposed as a promising treatment strategy for EPC. High levels of tumor necrosis factor-related weak inducer of apoptosis (TWEAK) have been reported in AMI, although its effect on EPCs has not been reported. In the present study, immunofluorescence and flow cytometry were performed to assess the effect of TWEAK in isolated mouse EPCs.

Kallistatin Inhibits Atherosclerotic Inflammation by Regulating Macrophage Polarization.

Kallistatin (KS) has been recognized as a plasma protein with anti-inflammatory functions. Macrophages are the primary inflammatory cells in atherosclerotic plaques. However, it is unknown whether KS plays a role in macrophage development and the pathogenesis of atherosclerosis.

Long term prognosis of acute coronary syndrome with chronic renal dysfunction treated in different therapy units at department of cardiology: a retrospective cohort study.

Coronary care unit is common in hospitals and clinical centers which offer intensive care and therapy for severe coronary artery disease patients. However, if coronary care unit could improve the long term prognosis of acute coronary syndrome patients with renal dysfunction remain unknown. Accordingly, we designed this study to evaluate the differences of incidence of major adverse cardiovascular events for acute coronary syndromes patients with renal dysfunction who treated in coronary care unit or normal unit.

Transplantation of bradykinin-preconditioned human endothelial progenitor cells improves cardiac function via enhanced Akt/eNOS phosphorylation and angiogenesis.

This study determines whether preconditioning (PC) of human endothelial progenitor cells (hEPCs) with bradykinin promotes infarcted myocardium repair via enhanced activation of B2 receptor (B2R)-dependent Akt/eNOS and increased angiogenesis. hEPCs with or without bradykinin preconditioning (BK-PC) were transplanted into a nude mouse model of acute myocardial infarction. Survival of transplanted cells was assessed using DiD-labeled hEPCs.

Transplantation of bradykinin-preconditioned human endothelial progenitor cells improves cardiac function via enhanced Akt/eNOS phosphorylation and angiogenesis.

This study determines whether preconditioning (PC) of human endothelial progenitor cells (hEPCs) with bradykinin promotes infarcted myocardium repair via enhanced activation of B2 receptor (B2R)-dependent Akt/eNOS and increased angiogenesis. hEPCs with or without bradykinin preconditioning (BK-PC) were transplanted into a nude mouse model of acute myocardial infarction. Survival of transplanted cells was assessed using DiD-labeled hEPCs.

[Impact and related mechanisms of stromal cell-derived factor-1α on serum deprivation-induced cardiac stem cells apoptosis].

Objective: To explore the impact and related mechanisms of stromal cell-derived factor-1α (SDF-1α) on serum deprivation-induced apoptosis of cardiac stem cells (CSCs).

Methods: CSCs were isolated from adult mouse heart tissue and cultured in vitro. Obtained cells were purified using magnetic-activated cell sorting (MACS) with c-kit magnetic beads.

Bradykinin preconditioning improves therapeutic potential of human endothelial progenitor cells in infarcted myocardium.

Objectives: Stem cell preconditioning (PC) is a powerful approach in reducing cell death after transplantation. We hypothesized that PC human endothelial progenitor cells (hEPCs) with bradykinin (BK) enhance cell survival, inhibit apoptosis and repair the infarcted myocardium.

Methods: The hEPCs were preconditioned with or without BK.

Tissue kallikrein-modified human endothelial progenitor cell implantation improves cardiac function via enhanced activation of akt and increased angiogenesis.

Endothelial progenitor cells (EPCs) have been shown to enhance angiogenesis not only by incorporating into the vasculature but also by secreting cytokines, thereby serving as an ideal vehicle for gene transfer. As tissue kallikrein (TK) has pleiotropic effects in inhibiting apoptosis and oxidative stress, and promoting angiogenesis, we evaluated the salutary potential of kallikrein-modified human EPCs (hEPCs; Ad.hTK-hEPCs) after acute myocardial infarction (MI).

Hypoxic preconditioning improves survival of cardiac progenitor cells: role of stromal cell derived factor-1α-CXCR4 axis.

Background: Cardiac progenitor cells (CPCs) have been shown to be suitable in stem cell therapy for resurrecting damaged myocardium, but poor retention of transplanted cells in the ischemic myocardium causes ineffective cell therapy. Hypoxic preconditioning of cells can increase the expression of CXCR4 and pro-survival genes to promote better cell survival; however, it is unknown whether hypoxia preconditioning will influence the survival and retention of CPCs via the SDF-1α/CXCR4 axis.

Methods And Results: CPCs were isolated from adult mouse hearts and purified by magnetic activated cell sorting using c-kit magnetic beads.

In vivo imaging of macrophages during the early-stages of abdominal aortic aneurysm using high resolution MRI in ApoE mice.

Background: Angiotensin II (ANG II) promotes vascular inflammation and induces abdominal aortic aneurysm (AAA) in hyperlipidemic apolipoprotein E knock-out (apoE(-/-)) mice. The aim of the present study was to detect macrophage activities in an ANG II-induced early-stage AAA model using superparamagnetic iron oxide (SPIO) as a marker.

Methodology/principal Findings: Twenty-six male apoE(-/-) mice received saline or ANG II (1000 or 500 ng/kg/min) infusion for 14 days.

Tissue kallikrein promotes cardiac neovascularization by enhancing endothelial progenitor cell functional capacity.

Tissue kallikrein (TK) has been demonstrated to improve neovasculogenesis after myocardial infarction (MI). In the present study, we examined the role and underlying mechanisms of TK in peripheral endothelial progenitor cell (EPC) function. Peripheral blood-derived mononuclear cells containing EPCs were isolated from rat.

Analysis of in situ and ex vivo αVβ3 integrin expression during experimental carotid atherogenesis.

Objective: Mural inflammation has been shown to contribute to the development of plaque, with the α(V)β(3) integrin highly expressed in atherosclerotic plaques. We herein examined α(V)β(3) integrin expression as a function of carotid atherosclerosis formation in the apolipoprotein E-deficient (apoE(-/-)) mouse.

Methods And Results: Constrictive collars were placed around the left common carotid arteries of apo E(-/-) mice maintained on a high-fat diet (n = 14).

Dual-modal tracking of transplanted mesenchymal stem cells after myocardial infarction.

Purpose: Results for implantation efficiency and effective improvement of cardiac function in the field of mesenchymal stem cells (MSCs) are controversial. To attempt to clarify this debate, we utilized magnetic resonance imaging (MRI) and near-infrared optical imaging (OI) to explore the effects of different delivery modes of mesenchymal stem cells on cell retention time and cardiac function after myocardial infarction (MI).

Methods: Rat MSCs were labeled with superparamagnetic iron oxide nanoparticles and 1, 1'-dioctadecyl-3,3,3',3'-tetramethylindodicarbocyanine, 4-chlorobenzenesulfonate salt (DiD) for noninvasive cell tracking in a rat MI model.

Vasculoprotective effects of rosiglitazone through modulating renin-angiotensin system in vivo and vitro.

Background: The peroxisome proliferator-activated receptor-γ (PPARγ) agonist rosiglitazone has been suggested to exert cardiovascular protection through the improvement of lipid metabolism, anti-inflammation, anti-proliferation etc. However, whether renin-angiotensin system (RAS) is involved in the vascular protective effects of PPARγ agonists is not fully understood. The present study aimed to investigate the effects of the renin-angiotensin system in vascular protection mediated by PPARγ agonists.